Adenosine receptor dependent signaling is not obligatory for normobaric and hypobaric hypoxia-induced cerebral vasodilation in humans

Hypoxia increases cerebral blood flow (CBF) with the underlying signaling processes potentially including adenosine. A randomized, double-blinded, placebo controlled design, was implemented to determine if adenosine receptor antagonism (theophylline, 3.75 mg/Kg) would reduce the CBF response to normobaric and hypobaric hypoxia. In 12 participants the partial pressures of end-tidal oxygen (P_ETO₂) and carbon dioxide (P_ETCO₂), ventilation (pneumotachography), blood pressure (finger-photoplethysmography), heart-rate (electrocardiogram), CBF (duplex ultrasound), and intra-cranial blood velocities (transcranial Doppler ultrasound) were measured during five-minute stages of isocapnic hypoxia at sea-level (98, 90, 80, & 70% SaO₂). Ventilation, P_ETO₂ and P_ETCO₂, blood pressure, heart-rate and CBF were also measured upon exposure (128±31 minutes following arrival) to high-altitude (3800m) and six-hours following theophylline administration. At sea-level, although the CBF response to hypoxia was unaltered pre/post placebo, it was reduced following theophylline (P<0.01); a finding explained by a lower P_ETCO₂ (P<0.01). Upon mathematical correction for P_ETCO₂, the CBF response to hypoxia was unaltered following theophylline. Cerebrovascular reactivity to hypoxia (i.e. response slope) was not different between trials, irrespective of P_ETCO₂. At high-altitude, theophylline (n=6) had no effect on CBF compared to placebo (n=6) when end-tidal gases were comparable (P>0.05). We conclude that adenosine receptor dependent signaling is not obligatory for cerebral hypoxic vasodilation in humans.

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